But it is not just the collaborations between African and European genes that are highlighted by the portraits. Another of my DNA volunteers, “Holly Golightly,” a distinguished African American biographer whom I met while she was on sabbatical in Oxford, was surprised when I told her that both copies of her lactase genes, located on chromosome 2, were inherited from Native American ancestors. She is lactose intolerant and had always put this down to her African background, whereas in fact her inability to break down lactose, which is found mainly in milk, is due to the poorly functioning lactase genes that she inherited from her Native American ancestors.
Possibly the most revealing feature of the chromosome portraits concerns the genes for the one trait that, more than any other has been used to define racial categories—that of color. All pigmentation in humans is due to just one basic substance, melanin. It alone is responsible for the vast range of skin and hair colors found in people from around the world. Melanin itself is a polymer derived from the amino acid tyrosine and is contained within pigmented cells, the melanocytes, in discrete granules. Basically, the more melanocytes and the more melanin in the granules, the darker the skin, eyes, and hair. Blue eyes are not blue because they contain a pigment but because, in the absence of melanin, light reflected from a layer in the iris is diffracted through the regularly spaced transparent collagen fibers in the cornea and gives the appearance of being blue; it is the same optical mechanism that imparts the vivid colors of a butterfly’s wing.
The genetic control of skin and hair pigmentation is orchestrated by eleven genes that we know about, though there may well be more. They each control different parts of the process of producing melanin granules and regulating the number of melanocytes. The paler end of the wide range of human pigmentation is probably a response to the reduced exposure to sunlight that some of our ancestors experienced when moving from Africa to higher latitudes. Some vital functions, like the synthesis of vitamin D and folic acid, depend on sunlight, so it makes sense that evolutionary natural selection would have promoted the survival of lighter-skinned individuals. When we look at the chromosome portraits, it is very clear that many of my African American volunteers, who count themselves as black, actually have a mixture of pigmentation genes from many different ancestries. To take just one example, the radio-talk-show host Mark Thompson. Of his eleven pigmentation genes, only two are of completely African origin, five have been inherited equally from European and African ancestors, two are an equal mix of African and Native American, and one has been inherited from exclusively European ancestors. That blend of origins is the direct result of the mixing of his chromosome segments in generations of his African, European, and Native American ancestors.
Since this process is more or less completely random, a vast number of combinations is possible in any African American. There will be individuals who actually have very little DNA from African ancestors, yet if these contributions include chromosome segments housing the pigmentation genes, then they will have typically dark coloring. Likewise there will be Americans whose DNA is almost all African in origin, yet if the pigmentation genes are not included in these segments and instead come from European ancestors, then their coloring will be white. Similarly, it would be entirely possible for a European American with only a small overall component of African DNA to be very dark skinned if these ancestral segments were to include the pigmentation genes. Our only Cherokee volunteer probably had a dark skin tone because the sole surviving segment of Native American DNA in his genome included one of the most influential of the pigmentation genes, located on chromosome 15.
As you leave the gallery, my hope is that you will come away with the feeling that you have glimpsed another world. A world that mocks the artificial divisions we have created for ourselves. A world made up of the corpuscles of DNA that each of us has inherited over millennia from our myriad ancestors, every one of them a resourceful survivor from earlier times. We are their privileged custodians in this world for a few short years, messengers through time to generations not yet born. Let us enjoy this honor while we may.
Acknowledgments
So many people have contributed to DNA USA, but let me start by thanking all the volunteers who either allowed me to sample their DNA or shared with me the results of earlier genetic analyses. Without their help there would simply have been nothing to write about. They are, in no particular order, Meriwether Schmid, Christopher Childs, Brenton Simons, Richard Ferguson, Dr. Henry Louis Gates Jr., Dr. Gretchen Holbrook Gertzina, Polly Furbush, Dr. Esteban Burchard, Dr. Roy King, Dr. Rick Kittles, Gina Paige, David Dearborn, Bonnie Healy, Dr. Nanibaa’ Garrison, Dr. Justin Barrett, Barbara Poole, Charlie Coleman, Doug Chase, Aaron Gray, Margaretta Barley, Lynda Duncan, Latonya Raston, Justin Connors, Rev. Mark Thompson, Toby Cooper, Brinson Weeks, Sandi Hewlett, Dr. Jay Lewis, and Lee Huntley.
Many people helped by giving up their valuable time to meet or talk with me, including Bennett Greenspan of Family Tree DNA, Dr. Rick Kittles and Gina Paige from African Ancestry, and Dr. Scott Woodward from the Sorenson Institute. I also enjoyed and benefited from conversations with Dr. Kimberly TallBear from the University of California, Berkeley; Dr. Gabrielle Tayac of the National Museum of the American Indian, Washington D.C.; Dr. Mike Hammer from the University of Arizona, Tucson; Anna Silas from the Hopi Cultural Center, Second Mesa, Arizona; Michael Markley, tribal historian of the Seaconke Wampanoag; Juan Luis Castro Suarez, lexicographer and restaurateur; and Serle Chapman, our guide in Wyoming, who provided a wise introduction to the Cheyenne.
I am very grateful for the enthusiastic help with the genome analyses and chromosome painting from 23andMe, Inc. in Mountain View, California—in particular, Dr. Joanna Mountain, Dr. Mike MacPherson, Stewart Ellis, and Linda Avey. Many people made what seemed at first a mammoth task come to completion by their generous welcome and support. I especially want to pay tribute to the New England Historic Genealogy Society, who enthusiastically supported and welcomed me, and my intrepid team of researchers, to their headquarters in Boston. A big thank-you to all the staff at NEHGS and particularly to the president and C.E.O., Brenton Simons; Kelly McCoulf, his tireless PA; and Lynn Betlock, who organized the DNA kits and the recruitment of New England volunteers. Also in Boston, or at least in nearby Cambridge, I owe a great deal to Dr. Henry Louis Gates Jr. and the staff at the W.E.B DuBois Institute for African and African American Studies at Harvard for their most generous hospitality.
All that research and travel had to be turned into a book, and for that I am very grateful to Robin Roberts-Gant and Gerry Black for their invaluable and skillful assistance with the book illustrations. The travel plans were also sometimes complicated, so I owe a lot to Debs Hull of Oxonian Travel, for smoothing the way, and, as so often, to the irreplaceable Hilary Prince and the very talented Mr. Bentley for holding the fort in Oxford while I was in America.
But no book is ever written without encouragement, and for this I must once again thank my literary agent, Luigi Bonomi, and, even more than usual, my editor at W. W. Norton, Bob Weil, whose idea it was in the first place and who, with Philip Marino’s editorial help, Sue Llewellyn’s and Don Rifkin’s copyediting (and translation into American), Chris Carruth’s index, Devon Zahn’s production skills, and Susan Foden’s proofreading, molded my rough and ready manuscript into the finished product.
Lastly, there would simply be no DNA USA without Ulla and Richard, who traveled with me over many thousands of miles by road, rail, and air; helped with the sample collection, voice recordings, note taking, and in so many other ways. With Richard’s sketches and Ulla’s constant encouragement, they made sure the book was finished in style, and on time.
Appendix
NATIVE AMERICAN
Core mutations of Native American mDNA clusters
CLUSTER
MUTATIONS
A1
223 390 319 362
A2
111 223 290 319 362
B
189 217
C
223 298 325 327
D
223 325 362
X
223 278
Calibrated origin dates and clan mother names for Native American mDNA clusters
CLUSTER
MOTHER
AGE (YRS)
A
Aiyana
15,800
B
Ina
18,700
C
Chochmingwu
19,600
D
Djigonese
16,900
X
Xenia
15,800
EUROPEAN
Calibrated origin dates, clan mother names, and frequencies for native European mDNA clusters
CLUSTER
FREQUENCY (%)
MOTHER
AGE (YRS)
U5
5.7
Ursula
47,000
HV
5.4
HV
34,000
X (I)
1.7
Xenia
26,000
U4
3.0
Ulrike
20,000
H
37.7
Helena
14,000
T
2.2
Tara
13,000
K
4.6
Katrine
12,500
T2
2.9
Tara
12,000
J
6.1
Jasmine
8,500
T1
2.2
Tara
9,000
AFRICAN
Clan mothers and ages of native African mDNA clusters
NOTATION
CLAN MOTHER
AGE (YRS)
Superclan L1
L1A
Layla
40,000
L1B
Lamia
30,000
L1C
Lalamika
60,000
L1D
Latasha
50,000
L1E
Lalla
83,000
L1F
Labana
86,000
L1K
Lakita
92,000
Superclan L2
L2A
Leisha
55,000
L2B
Lesedi
32,000
L2C
Lingaire
27,000
L2D
Lindewe
122,000
Superclan L3
L3A
Lara
60,000
L3B
Limber
21,000
L3D
Lingaire
30,000
L3E
Lila
45,000
L3F
Lungile
36,000
L3G
Lubaya
45,000
Regional distribution within Africa of the most frequent native African mDNA clusters
REGION
TOP 5 MOST FREQUENT CLUSTERS
East
L1A, L2, L3A, L3F, L3G
Southeast
L1A, L2A1a, L2A1b, L3E
South
L1A, L1D, L1K, L3B, L3E
Central
L1A, L1C, L2A1, L3E
West
L1B, L2A1, L3B, L3D
North
L1B, L2A1, L3B, L3D
FROM
TO
MUTATIONS
Superclan L1
Root
L1
16230
Root
L1D
16129, 16243
L1D
L1D1
16294
L1D
L1D2
16234
Root
L1F
16169, 16327
Root
L1A
16129, 16148, 16172, 16188G, 16278, 16320
L1A
L1A1
16168
L1A1
L1A1a
16278
L1A
L1A2
16129
Root
L1K
16172, 16209, 16214, 16291
L1K
L1K1
16166C
Root
L1E
16129, 16148, 16166
L1E
L1E1
16111, 16254, 16311
L1E
L1E2
16355, 16362
L1
L1B/C
7055R
L1
L1B
16126, 16264, 16270
L1B
L1B1
16293
L1B/C
L1C
16129, 16294, 16360
L1C
L1C1
16293
L1C1
L1C1a
16274
L1C1a
L1C1a1
16214, 16223, 16234, 16249
L1C
L1C2
16265C, 16286G
L1C
L1C3
16187, 16215
L1
L2/3
16187, 16189, 16311
Superclan L2
L2/3
L2
16390
L2
L2C
13957R
L2C
L2C1
16318
L2C
L2C2
16264
L2
L2A
13803R, 16294
L2A
L2A1
16309
L2A1
L2A1a
16286
L2A1
L2A1b
16290
L2
L2D
3693R, 16399
L2D
L2D1
16129, 16189, 16223, 16300, 16354
L2D
L2D2
16111A, 16145, 16239, 16292, 16355
L2
L2B
4157R, 16129, 16114A, 16213
L2B
L2B1
16362
Superclan L3
L2/3
L3
3592R, 16278
L3
L3F
16209, 16311
L3F
L3F1
16292
L3
L3G
16293T, 16311, 16355, 16362
L3
L3B/D
16124
L3B/D
L3B
10084R, 16278, 16362
L3B
L3B1
16124
L3B
L3B2
16311
L3B/D
L3D
8616R
L3D
L3D1
16319
L3D
L3D2
16256
L3D
L3D3
16189, 16278, 16304, 16311
L3
L3E
2349R
L3E
L3E3/4
5260R
L3E3/4
L3E4
16264
L3E3/4
L3E3
16265T
L3E
L3E2
16320
L3E
L3E2b
16172, 16189
L3E
L3E1
16327
L3E1
L3E1a
16185
L3E1
L3E1b
16325
L3A
M
10397R
L3A
N
10871R
Mutations in the African mDNA tree.
Numbers are p
ositions of mutations in the mDNA sequence. Positions without a suffix are transitions. Suffixes A, G, C, T indicate transversions to these bases. Suffix del indicates a deletion while R is a restriction enzyme variant.
CLAN DONALD GENEALOGY
Identification of individuals on Clan Donald genealogy
(see Fig.2)
CODE
NAME
DATES
BRANCH
A
Somerled
c. 1100–1164
B
Dugall, founder of Clan Dougal of Lorne
c. 1118–?
C
Donald MacRanald of the Isles
1190–1269
D
Alastair Mor MacDonald, founder of Clan Alastair
d. 1299
E
John MacDonald, Lord of the Isles
d. 1386
F
Ranald Macdonald, 1st of Clanranald and Glengarry
d. 1386
G